A target role for mast cell in the prevention and therapy of hepatic fibrosis.

Hepatic fibrosis is a common pathological process of chronic hepatic disease. Despite the extensive studies, the pathophysiological mechanisms in hepatic fibrosis remain unclear. Mast cell has a variety of physiological and pathological functions through the production of heparin, histamine, neutrophil chemoattractants, immunoregulatory cytokines, and mast cell-specific serine proteases tryptase and chymase. The survival and proliferation of mast cell are dependent upon stem cell factor. More recently, the data have suggested that mast cell has been associated with hepatic fibrosis in many chronic liver diseases. However, to what extent the mast cell effects the hepatic fibrosis remains to be clarified. Several therapeutic approaches to inhibit mast cell activation have already demonstrated some clinical utility in tissue fibrosis or inflammatory diseases such as the use of mast cell stabilizers, inhibitors of tryptase or chymase, blockade of stem cell factor and anti-IgE therapy. The article introduces the hypothesis that mast cell has a central role when it is affected by its activation state in the progression of hepatic fibrosis, thus new therapeutic strategies for treatment of hepatic fibrosis are suggested by this hypothesis. Considering the important role of mast cell and the development of these tangible therapeutic approaches in hepatic fibrosis will enable us to target any types of chronic liver diseases, which appears to be a more reasonable or a promising strategy.